We evaluated the effects of nitric oxide (NO) on acetylcholine release and
the contractile response induced by electrical field stimulation in rabbit
bladder smooth muscles using a muscle bath and high performance liquid chro
matography coupled with microdialysis. Electrical field stimulation (supram
aximum voltage, pulse duration 0.5 ms, frequency 5 and 20 Hz) was applied t
o a smooth muscle strip isolated from rabbit bladder. With low-frequency (5
Hz) stimulation, pretreatment with N-infinity-nitro-L-arginine (L-NNA) (10
0 muM) significantly increased electrical field stimulation-induced acetylc
holine release and contractile response, which were reduced by the addition
of L-arginine. Pretreatment with sodium nitroprusside in the absence or pr
esence of L-NNA significantly decreased electrical field stimulation-induce
d acetylcholine release and contractile response. In contrast, with high fr
equency (20 Hz) stimulation, pretreatment with L-NNA and sodium nitroprussi
de had no significant effect on either contractile response or acetylcholin
e release. Pretreatment with sodium nitroprusside caused no significant cha
nges in carbachol and ATP-induced contractile responses. Sodium nitroprussi
de and L-NNA had no significant effects on the atropine-resistant part of t
he contraction induced by electrical field stimulation in rabbit bladder sm
ooth muscles. The results suggest that there is a NO-mediated mechanism inh
ibiting acetylcholine release from cholinergic nerve endings in rabbit blad
der, which may contribute to bladder function. (C) 2001 Elsevier Science B.
V. All rights reserved.